It was previously shown that in a strain of mice with hereditary vasopressin-resistant diabetes insipidus there is a specific defect in protein phosphorylation in renal medulla. Two specific phosphoproteins, of molecular weights 175,000 and 185,000, display markedly diminished phosphorylation in homogenates from severely affected mice. These phosphoproteins are present in the particulate fraction of renal medulla from several murine strains with normal concentrating ability, and are relatively specific for this tissue, being undetectable in renal cortex, liver or brain. Additional studies have utilized young mice of the DI strain and mildly affected older mice. In both the urinary concentrating ability is intermediate between that of normal and severely affected mice, and both display an intermediate capacity to phosphorylate the proteins of interest. This finding suggests that the defect in phosphorylation is not simply coinherited with nephrogenic diabetes insipidus, but is directly related to urinary concentrating ability.